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Prostaglandins in bone: bad cop, good cop?

期刊

TRENDS IN ENDOCRINOLOGY AND METABOLISM
卷 21, 期 5, 页码 294-301

出版社

ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tem.2009.12.004

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资金

  1. NIH [AR47673, DK48361, AR18063, F30 AG034013]
  2. NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR047673, R01AR018063, R01AR060286] Funding Source: NIH RePORTER
  3. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R56DK048361, R01DK048361] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE ON AGING [F30AG034013] Funding Source: NIH RePORTER

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Prostaglandins (PGs) are multifunctional regulators of bone metabolism that stimulate both bone resorption and formation. PGs have been implicated in bone resorption associated with inflammation and metastatic bone disease, and also in bone formation associated with fracture healing and heterotopic ossification. Recent studies have identified roles for inducible cyclooxygenase (COX)-2 and PGE2 receptors in these processes. Although the effects of PGs have been most often associated with cAMP production and protein kinase A activation, PGs can engage an extensive G-protein signaling network. Further analysis of COX-2 and PG receptors and their downstream G-protein signaling in bone could provide important clues to the regulation of skeletal cell growth in both health and disease.

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